(1981). A Comparative Study of the Toxicity of n-Pentane, n-Hexane, and n-Heptane to the Peripheral Nerve of the Rat. Clinical Toxicology: Vol. 18, No. 12, pp. 1395-1402.
The neurotoxicity of n-pentane, n-hexane, and n-heptane have been studied in Wistar strain male rats after exposure to 3000 ppm of n-pentane, n-hexane, or n-heptane for 12 hours a day for 16 weeks. The nerve conduction velocity and the distal latency were measured before the beginning of the exposure and after exposure for four, eight, 12, and 16 weeks. The experiment showed that n-hexane disturbed the conduction velocity of the motor nerve and the mixed nerve and prolonged the distal latency in the rat9s tail, but that n-pentane and n-heptane did not. The light and electron microscopic examination showed that the peripheral nerve, the neuromuscular junction, and the muscle fibre of the rats exposed to n-hexane were severely impaired, but those of the rats exposed to n-pentane or n-heptane showed no particular changes even after 16 weeks of exposure. These results show that n-hexane is far more toxic to the peripheral nerve of the rat than n-pentane or n-heptane. It is necessary to study the neurotoxicity of other petroleum hydrocarbons, since some reports suggest that petroleum solvents might possibly contain neurotoxic hydrocarbons other than n-hexane.
1-Bromopropane is used widely as an alternative to ozone-depleting solvents. The neurotoxic effects of this agent have been described in humans and experimental animals. Here we investigated the underlying mechanisms of the neurotoxic effects of 1-bromopropane by examining the initial biochemical changes in the central nervous system. Four groups of 9 Wistar male rats each were exposed to 200, 400, or 800 ppm 1-bromopropane or only fresh air, 8 h per day for 7 days. At the end of the experiment, the cerebrum, cerebellum, brain stem and lumbar enlargement of the spinal cord were dissected out from each rat (n = 8) for biochemical analyses. Morphological examinations of the nervous system were performed in the remaining rat of each group. 1-Bromopropane dose-dependently decreased neurospecific gamma-enolase, total glutathione, and nonprotein sulfhydryl groups in the cerebrum and cerebellum. Creatine kinase activity decreased dose-dependently in the brain and spinal cord. Histopathological examination showed swelling of preterminal axons in gracile nucleus and degeneration of myelin in peripheral nerves. Our results of low levels of gamma-enolase suggested that 1-bromopropane might primarily cause functional or cellular loss of neurons in the cerebrum and cerebellum. Glutathione depletion or modification to functional proteins containing a sulfhydryl base as a critical site might be the underlying mechanism of 1-bromopropane neurotoxicity.
This study was intended to determine whether or not methyl ethyl ketone (MEK) enhances the neurotoxicity of n-hexane at low concentration and after long term exposure. Separate groups of eight rats were exposed to 100 ppm n-hexane, 200 ppm MEK, 100 ppm n-hexane plus 200 ppm MEK, or fresh air in an exposure chamber for 12 hours a day for 24 weeks. The body weight, motor nerve conduction velocity (MCV), distal motor latency (DL), and mixed nerve conduction velocities (MNCVs) were measured before exposure and after four, eight, 12, 16, 20, and 24 weeks9 exposure. One rat of each group was histopathologically examined after 24 weeks9 exposure. Exposure of 100 ppm n-hexane did not significantly decrease the functions of the peripheral nerve throughout the experiment. Exposure to 200 ppm MEK significantly increased MCV and MNCVs and decreased DL after four weeks9 exposure, but at this later stage no significant changes were found throughout the experiment by comparison with the controls. Mixed exposure to 100 ppm n-hexane plus 200 ppm MEK significantly decreased by comparison with the controls. On histopathological examination of the tail nerve, however, no changes were found in any of the exposed groups or the controls. These results suggest that MEK might enhance the neurotoxicity of n-hexane at a low concentration, and mixed exposures to n-hexane and MEK should be avoided.
The unique border zone between the zona fasciculata and z. reticularis of the female adrenal cortex is formed in the wild-colored inbred mastomys (Praomys coucha) strain, MWC, but never in the chamois-colored inbred strain, MCC. This clear strain-specific trait was genetically analyzed using F1, F2, and backcross progenies produced between MWC and MCC. Reciprocal crosses gave no significant differences in the phenotypic ratio of F1 or F2 progeny. Border zone formation was detected in 0% of F1 females, 25.8% of F2 females, 0% of backcross females between F1 and MCC, and 47.7% of backcross females between F1 and MWC. From these results, it was concluded that border zone formation in the female MWC adrenal is regulated by a single autosomal recessive gene and this gene was named bzf (border zone formation).
